Immunohistochemical Profile and Fluorescence In Situ
Hybridization Analysis of Diffuse Large B-Cell Lymphoma
in Northern China
Ting Li, MD; L. Jeffrey Medeiros, MD; Pei Lin, MD; Hongfang Yin, MD, PhD; Martin Littlejohn, BA; Whan Im, BA; P. Alan Lennon,
PhD; Peter Hu, PhD; Jeffrey L. Jorgensen, MD, PhD; Mei Liang, MD, PhD; Hua Guo, MD; C. Cameron Yin, MD, PhD
NContext.—Gene expression profiling of diffuse large B-
cell lymphoma using complementary DNA microarrays has
revealed 2 major prognostic groups in Western countries:
germinal center B-cell–like and nongerminal center B-cell–
like lymphomas. Immunohistochemical analysis using
antibodies specific for CD10, BCL6, and MUM1 has been
proposed as a surrogate for gene expression profiling.
Objective.—To study the immunohistochemical features
of diffuse large B-cell lymphoma cases from northern
China because geographic differences for this disease are
known to exist.
Design.—Morphologic, immunohistochemical, and fluo-
rescence in situ hybridization analyses of 63 cases of
diffuse large B-cell lymphoma from northern China.
Results.—There were 38 men and 25 women with a
median age of 57 years (range, 12–87 years). CD10 was
positive in 19 cases (30%), BCL6 was positive in 22 cases
(35%), and MUM1 was positive in 32 cases (51%).
Twenty-one (33%) cases were germinal center B-cell–like
lymphoma, and 42 (67%) were nongerminal center B-cell–
like lymphoma. BCL2 was expressed more often in
nongerminal center B-cell–like disease versus germinal
center B-cell–like disease (60% versus 24%, P = .01) and
in nodal versus extranodal (64% versus 30%, P = .01)
cases. Fluorescence in situ hybridization analysis showed
BCL6, MYC, and BCL2 rearrangements in 11 of 32 (34%),
8 of 27 (30%), and 11 of 50 (22%) cases, respectively.
Conclusions.—These results add to what is known about
the geographic variation of diffuse large B-cell lymphomas.
In northern China, the frequency of the germinal center B-
cell–like type and BCL6 expression and/or BCL6 rear-
rangement is less and the frequency of MYC rearrangement
is greater than have been reported in Western countries.
(Arch Pathol Lab Med. 2010;134:759–765)
Western countries, and its frequency is even higher in
Asia.1Diffuse large B-cell lymphoma, as a diagnostic
category, displays striking heterogeneity at the clinical,
histologic, immunophenotypic, and molecular levels. At
the DNA level, abnormalities of BCL6 at band 3q27, of
BCL2 at band 18q21, and of MYC at band 8q24 have been
described in 45%, 20%, and 15% of cases, respectively.2At
the RNA level, gene expression profiling using comple-
mentary DNA (cDNA) microarrays has shown that
DLBCL consists of molecularly distinct subgroups.3–7In
studies from the National Institutes of Health, 3 sub-
groups were reported.4One subgroup, termed germinal
center B-cell–like (GCB) type, expresses genes characteristic
of normal germinal center B cells. A second group,
iffuse large B-cell lymphoma (DLBCL) constitutes
30% to 40% of adult non-Hodgkin lymphomas in
designated activated B-cell–like type, expresses genes
characteristic of activated peripheral blood B cells and
plasma cells. A third group, type C, has neither a GCB nor
an activated B-cell–like signature. These authors have
further shown that these signatures have prognostic
meaning. Patients with a GCB tumor have a relatively
good prognosis following chemotherapy. In contrast,
patients with an activated B-cell–like or a type C DLBCL
have a similar, poorer prognosis and, thus, can be grouped
Although gene expression profiling studies analyze
thousands of genes, it seems highly likely that DLBCL
subgroups can be distinguished with a smaller panel of
genes. Rosenwald and Staudt8suggested that as few as 13
to 17 genes can be used to identify these prognostically
different subgroups. Lossos and colleagues9have recom-
mended a panel of 6 genes. Nevertheless, gene expression
profiling technology is not currently available for routine
clinical use in many institutions. Others have suggested
that selected markers assessed by routine immunohisto-
chemistry can be used as a surrogate for gene expression
profiling.6–10A number of algorithms have been proposed,
but the most widely used is that suggested by Hans and
colleagues.10In this system, a GCB tumor is CD10+or
CD102/BCL6+/MUM12, and a non-GCB tumor is CD102/
BCL62or CD102/BCL6+/MUM1+. In their study, the
immunohistochemical (IHC) profile correctly predicted
Accepted for publication July 8, 2009.
From the Department of Pathology, First Hospital of Peking
University, Beijing, China (Drs Li, H. Yin, and Guo); and the
Department of Hematopathology (Drs Medeiros, Lin, Jorgensen, Liang,
and C. C. Yin) and the Molecular Genetic Technology Program (Messrs
Littlejohn and Im and Drs Lennon and Hu), University of Texas M. D.
Anderson Cancer Center, Houston.
The authors have no relevant financial interest in the products or
companies described in this article.
Reprints: C. Cameron Yin, MD, PhD, Department of Hematopathol-
ogy, Unit 72, University of Texas M. D. Anderson Cancer Center, 1515
Holcombe Blvd, Houston, TX 77030 (e-mail: email@example.com).
Arch Pathol Lab Med—Vol 134, May 2010 IHC and FISH Analysis of DLBCL in Northern China—Li et al759
the gene expression profile in approximately 75% of cases.
In Western countries approximately 40% to 60% of DLBCL
cases are the GCB type.7,10,11
There is considerable variation in the incidence rates of
non-Hodgkin lymphomas worldwide.12,13For example,
follicular lymphoma is more common in North America
and Western Europe than in most Asian countries.13–15The
frequency of t(14;18)(q32;q21)/BCL2–IGH is significantly
higher in follicular lymphomas arising inthe United States
than in Asian populations.16These findings suggest that
follicular lymphoma may be a heterogeneous disease
because of geographic factors and encompasses entities
with distinct molecular pathogenesis, in particular, the
BCL2 rearrangement status and different etiologic or
genetic factors and, potentially, distinct clinical manifes-
tations and natural history. Similar geographic differences
are likely to exist for other types of lymphomas.
In this study, we profiled 63 cases of DLBCL from
northern China to compare with what has been reported
in the literature for DLBCL in the United States or other
Western countries. In each case, we assessed the cytologic
features and used the Hans et al10IHC system to classify
these cases into GCB and non-GCB types. We also
assessed a number of other IHC markers and used
fluorescence in situ hybridization (FISH) to assess BCL6,
BCL2, and MYC rearrangements. To our knowledge, this
is one of the largest studies on DLBCL from China.
MATERIALS AND METHODS
The study was conducted according to an institutional review
board–approved laboratory protocol and followed the provisions
of the Helsinki accord. The files of the Department of Pathology,
the First Hospital of Peking University (Beijing, China) from
January 2000 through December 2005 were searched for cases of
DLBCL. Seventy-two cases were identified. The diagnosis of
DLBCL was based on histologic and immunophenotypic
findings using the criteria of the World Health Organization
classification.1Cases with insufficient paraffin-embedded blocks
were excluded, leaving a study group of 63 cases. Clinical
information was obtained by review of the hospital-based
medical records. Hematoxylin-eosin–stained slides, routinely
prepared from formalin-fixed, paraffin-embedded tissue sec-
tions, were reviewed.
To construct tissue microarrays, 4 representative 0.6-mm cores
of each tumor were selected from the formalin-fixed, paraffin-
embedded tissue blocks andwere relocated using a tissue arrayer
(Beecher Instruments, Silver Spring, Maryland). Tissue sections
of 5 mm thickness were then cut from the arrays using a standard
microtome for immunohistochemistry and FISH.
Immunohistochemical analysis was performed using forma-
lin-fixed, paraffin-embedded tissue sections, an avidin-biotin-
peroxidase complex method, and an automated immunostainer
(Ventana-Biotech, Tucson, Arizona) as described previously.17
All tissue sections underwent heat-induced antigen retrieval. The
antibodies were specific for CD5 (Labvision/Neomarker, Mon-
treal, Quebec, Canada), CD10 (Novocastra/Vision Biosystem,
Benton Lane, Newcastle upon Tyne, United Kingdom), CD20
(Dako, Carpinteria, California), CD30 (Dako), CD138 (Serotec,
Raleigh, North Carolina), PAX5 (Transduction Labs, San Diego,
California), BCL2 (Novocastra/Vision Biosystem), BCL6 (Dako),
MUM1 (Santa Cruz Biotechnology, Santa Cruz, California), ALK
(Dako), MIB-1 (Ki-67, Dako), p53 (Dako), and p63 (clone 4A4,
Santa Cruz Biotechnology). Clone 4A4 recognizes both the
transactivating and truncated p63 isoforms.
The IHC results for CD10, BCL2, BCL6 and MUM1 were
designated as positive or negative according to the criteria
defined by Hans et al,10with a cutoff level of 30%. Results of IHC
studies for other antibodies were semiquantitatively scored as
negative (2, ,5% cells positive), weakly positive (1+, 5% to ,25%
cells positive), moderately positive (2+, 25%275% cells positive),
or strongly positive (3+, .75%2100% cells positive). The
percentage of Ki-67+cells was estimated to the nearest 10% (ie,
10%, 20%, 30%, etc). Only nuclear staining was regarded as
positive for Ki-67, PAX5, BCL2, p53, and p63. For all cases, both
hematoxylin-eosin–stained and immunohistochemical slides
were reviewed independently by 2 pathologists. Discordant
interpretations were resolved by review at a multiheaded
Using the algorithm of Hans et al,10cases were designated as
GCB if CD10 was positive, or as non-GCB if both CD10 and BCL6
were negative. If CD10 was negative and BCL6 was positive, the
expression of MUM1 determined the subclassification: if MUM1
was negative, the case was assigned to the GCB subgroup; if
MUM1 was positive, the case was assigned to the non-GCB
In Situ Hybridization
In situ hybridization analysis for Epstein-Barr virus–encoded
small RNA (EBER) was performed using formalin-fixed, paraf-
fin-embedded tissue sections, a fluorescein-labeled peptide
nucleic acid probe, and the Novocastra in situ hybridization kit
(NCL-EBV-K) according to the manufacturer’s instructions, with
the appropriate positive and negative control samples.
Fluorescence In Situ Hybridization
Interphase FISH analysis was performed on tissue microarrays
sections using dual-color, break-apart probes specific for BCL2,
BCL6, and MYC (Abbott Laboratories, Des Plaines, Illinois) as
previously reported.18Briefly, formalin-fixed, paraffin-embed-
ded tissue microarrays sections were deparaffinized using the
Paraffin Pretreatment Kit II (Abbott) according to the manufac-
turer’s instructions. Following hybridization with the above
FISH probes, the slides were analyzed using a Zeiss Axiophot
fluorescent microscope including single- and triple-band pass
filters (Welwyn, Garden City, Herts, United Kingdom). One
hundred intact, nonoverlapping nuclei were assessed by 2
independent investigators (200 total), and the percentages of
positive nuclei were averaged. The positive cutoff value used
was 8% for all FISH probes. Digital images were captured by a
Power Macintosh G3 System and MacProbe version 4.4 (Applied
Imaging, San Jose, California).
The Fisher exact test was used to compare differences between
various subgroups. The results were considered statistically
significant when P , .05.
The study group included 38 men and 25 women with a
median age of 57 years (range, 12–87 years). The series
included 33 nodal (52%) and 30 extranodal (48%) DLBCLs.
The distribution of extranodal sites was stomach (n 5 9,
30%),smallintestine (n56, 20%),brain (n 54, 13%),colon
(n 5 3, 10%), tonsil (n 5 3, 10%), thyroid gland (n 5 2, 7%),
spleen (n 5 1, 3%), breast (n 5 1, 3%), and testis (n 5 1,
Histologic sections of all 63 cases showed diffuse
infiltration by large lymphoid cells. According to the
760Arch Pathol Lab Med—Vol 134, May 2010IHC and FISH Analysis of DLBCL in Northern China—Li et al
World Health Organization classification,1these cases
were subclassified as follows: (1) centroblastic (n 5 50,
79%), composed of medium-sized to large lymphoid
cells with round to oval, vesicular nuclei, fine chroma-
tin, 2 to 4 membrane-bound nucleoli, and scant
amphophilic cytoplasm (Figure 1, A); (2) immunoblastic
(n 5 4, 6%), in which greater than 90% of the neoplastic
cells were immunoblasts with prominent, centrally
located nucleoli and appreciable basophilic cytoplasm
(Figure 1, B); (3) anaplastic (n 5 3, 5%), characterized by
very large round, oval, or polygonal cells with bizarre
pleomorphic nuclei, some of which resembled Reed-
Sternberg cells (Figure 1, C). In addition, 6 cases (10%)
of DLBCL in this study were large-cell transformation of
extranodal (gastrointestinal tract) marginal zone B-cell
(MALT lymphoma). These neoplasms were character-
ized by the presence of sheets of large cells with
irregular nuclear contours and abundant eosinophilic
cytoplasm in a background of low-grade MALT lym-
phoma (Figure 1, D). The distribution of these variants
is summarized in Table 1.
Among the 33 cases of nodal DLBCL, 29 (88%) were
centroblastic, 3 (9%) were immunoblastic, and 1 (3%) was
anaplastic. Among the 30 cases of extranodal DLBCL, 21
(70%) were centroblastic, 2 (7%) were anaplastic, and 1
anaplastic; D, arising from low-grade marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT-L) lymphoma (hematoxylin-
eosin, original magnification 3500).
Morphologic variants of cases of diffuse large B-cell lymphoma (DLBCL) from northern China: A, centroblastic; B, immunoblastic; C,
Table 1. Morphologic Features of 63 Cases of Diffuse Large B-Cell Lymphoma From China
Type CB, No. (%)IB, No. (%) Anaplastic, No. (%)MALT-L, No. (%)Total, No. (%)
Abbreviations: CB, centroblastic; IB, immunoblastic; MALT-L, diffuse large B-cell lymphoma associated with low-grade marginal zone B-cell
lymphoma of mucosa-associated lymphoid tissue.
Arch Pathol Lab Med—Vol 134, May 2010 IHC and FISH Analysis of DLBCL in Northern China—Li et al761
(3%) was immunoblastic. The other 6 (20%) cases were
associated with MALT lymphoma. A starry sky pattern
was observed in 4 DLBCLs (6%); all were centroblastic.
Marked apoptosis or necrosis was noted in 4 cases (6%),
and prominent sclerosis was identified in 2 cases (3%).
All cases showed moderate (2+) to strong (3+) expression
of CD20 and PAX5 and were negative for CD3, supporting
B-cell lineage. Three cases (5%) of anaplastic DLBCL
demonstrated moderate to strong positivity for CD30.
CD5 was positive in 3 centroblastic cases (5%). Scattered
CD138-immunoreactive cells were seen in 1 (2%) centro-
blastic tumor. All cases were negative for ALK.
The results of IHC staining for CD10, BCL2, BCL6, and
MUM1 are summarized in Table 2. MUM1 was expressed
in 32 (51%), BCL6 in 22 (35%), and CD10 in 19 (30%) of the
cases. Based on the results of IHC studies for the above 3
markers, the cases were subclassified into 2 groups: GCB
and non-GCB. Twenty-one (33%) were GCB, and 42 (67%)
were non-GCB. Among the 21 GCB cases, 10 (48%)
expressed both CD10 and BCL6 (CD10+/BCL6+/MUM1+,
n 5 6; or CD10+/BCL6+/MUM12, n 5 4); 9 (43%)
expressed CD10 alone (CD10+/BCL62/MUM12); and 2
(10%) expressed BCL6 alone (CD102/BCL6+/MUM12).
Among the 42 non-GCB cases, 16 (38%) expressed MUM1
alone (CD102/BCL62/MUM1+), 16 (38%) were negative
for all 3 markers (CD102/BCL62/MUM12), and 10 (24%)
MUM1+). MUM1 was expressed more often in nodal (22
of 33; 67%) than in extranodal (10 of 30; 30%; P 5 .01)
DLBCLs. No significant differences in the expression of
Table 2. Immunophenotypic Features of 63 Cases of Diffuse Large B-Cell Lymphoma From China
GCB, n = 21,
Non-GCB, n = 42,
Nodal, n = 33,
Extranodal, n = 30,
Abbreviation: GCB, germinal center B-cell–like type.
staining (original magnification 3200).
Immunohistochemical analysis using antibody specific for p63 showing negative (A), weak (B), moderate (C), and strong (D) positive
762 Arch Pathol Lab Med—Vol 134, May 2010 IHC and FISH Analysis of DLBCL in Northern China—Li et al
BCL6 or CD10 between nodal and extranodal cases were
observed (Table 2).
BCL2 expression was observed in 30 of 63 cases (48%),
of which, 25 (60%) were non-GCB and 5 (24%) were GCB
(P 5 .01). Twenty-one of 33 nodal cases (64%) were
positive, whereas 9 of 30 of the extranodal cases (30%)
were positive (P 5 .01).
Staining for p53 and p63 was predominantly nuclear
with occasional cytoplasmic staining. Thirty DLBCL cases
(48%) were positive for p53: 17 (27%) showed weak
staining, 8 (13%) had moderate staining, and 5 (8%) had
strong staining. Thirty-six DLBCL cases (57%) were
positive for p63: 15 (24%) showed weak staining, 18
(29%) had moderate staining, and 3 (5%) had strong
staining (Figure 2, A through D). Expression of both p53
and p63 was observed in 21 DLBCL cases (33%), including
10 GCB and 11 non-GCB types. Ki-67 showed a low
(,30%), moderate (30%–70%), or high (.70%) prolifera-
tion index in 22 (35%), 34 (54%), and 7 (11%) of cases,
respectively (Table 3).
In Situ Hybridization for EBER
Epstein-Barr virus–encoded small RNA (EBER) was
detected in 3 cases (5%) of DLBCL: 2 were nodal non-GCB
and 1 was an extranodal GCB type. In 2 of these tumors,
most cells were positive for EBER. In 1 case, a nodal non-
GCB DLBCL, only 5% of tumor cells were positive.
Fluorescence In Situ Hybridization for MYC, BCL2,
Fluorescence in situ hybridization analysis revealed
BCL6 rearrangement in 11 of 32 cases (34%) of DLBCL
(range of signals, 12%–55%; median, 46%). MYC was
rearranged in 8 of 27 cases (30%; range of signals, 8%–64%;
median, 27%), and BCL2 was rearranged in 11 of 50 cases
(22%; range of signals, 8%–56%; median, 11%) (Table 4;
Figure 3). No significant difference was noted in BCL6,
MYC, or BCL2 rearrangements between GCB and non-
GCB tumors or between nodal and extranodal DLBCL.
Three cases (2 non-GCB, 1 GCB) were positive for both
BCL2 and BCL6 rearrangements. One GCB case of DLBCL
was positive for both MYC and BCL2 rearrangements.
We studied the morphologic features, immunopheno-
typic profile, and FISH results in 63 cases of DLBCL from
northern China. Using the same algorithm proposed by
Hans et al,1021 tumors (33%) were of GCB and 42 (67%)
were of non-GCB type. The percentage of DLBCL cases
with a GCB immunophenotype in our series from China is
somewhat less than that reported in Western countries. In
various studies, the percentage of cases of GCB type has
ranged from 40% to 60%.7,10,11Similar to our results, 2
groups from Japan reported that the proportion of GCB
DLBCL ranged from 32% to 39%.19,20These results in
DLBCL from China are in keeping with the results in
Japanese patients. As many cases of DLBCL may be
preceded by, or are related to, follicular lymphoma, our
results are also in parallel with the lower frequency of
follicular lymphoma in Asian countries.21
The frequency of CD10 (30%) and MUM1 (51%)
expression in this study fell within ranges reported by
others of 25% to 50% and 47% to 54%, respectively.10,11
However, only 35% of lymphomas in our series expressed
BCL6, which is less than the lower end of the reported
range of 57% to 75% from Western countries.10,22Further-
more, only 34% of cases assessed showed BCL6 gene
rearrangement, which is also lower than the reported
frequency of 45%.2BCL6 is a zinc-finger protein that acts
as a transcriptional repressor. It is expressed in germinal
center B cells and in a subset of CD4+T cells23and plays a
critical role in germinal center formation.24We do not have
an explanation for the lower frequency of BCL6 rear-
rangement and expression in cases of Chinese DLBCL,
except to implicate geographic and genetic factors.
Because BCL6 gene abnormalities are common in DLBCL
seen in Western countries, the fewer BCL6 cases of
rearrangement and expression in Chinese DLBCL may
suggest that therapies targeted at the BCL6 pathway may
be less effective in Chinese patients.
No significant differences in BCL2 expression between
GCB and non-GCB types of DLBCL have been reported in
previous studies (50%–67% in GCB cases versus 45%–62%
in non-GCB cases).6,25Although the overall frequency of
BCL2 expression inour study(48%)fellwithinthe reported
Table 3.Staining Pattern of p53, p63, and Ki-67
p53, No. (%)p63, No. (%)Ki-67, No. (%)
Abbreviations: 2, negative; 1+, weakly positive; 2+, moderately positive; 3+, strongly positive; GCB, germinal center B-cell–like type.
Table 4. Fluorescence In Situ Hybridization Results of MYC, BCL2, and BCL6 Rearrangements
GeneTotal GCBNon-GCBPNodal ExtranodalP
Abbreviation: GCB, germinal center B-cell–like type.
Arch Pathol Lab Med—Vol 134, May 2010IHC and FISH Analysis of DLBCL in Northern China—Li et al763
range,BCL2 wasexpressed significantly more often innon-
GCB (60%) than in GCB cases (24%, P 5 .01) and in
significantly more nodal (64%) versus extranodal DLBCL
(30%, P 5 .01). However, no significant difference in the
frequency of BCL2 gene rearrangement was observed
between GCB and non-GCB cases. It has been suggested
that mechanisms other than t(14;18)(q32;q21), such as 18q21
amplification (where BCL2 gene resides) or activation of the
nuclear factor-kB pathway, may be primarily responsible
for the upregulation of BCL2 expression in the non-GCB
subgroup.26The prognostic role of BCL2 overexpression in
DLBCL is still controversial. Some groups using multivar-
iate analysis have suggested that BCL2 is the most
predictive prognostic marker.27Other groups have reported
that there is no significant correlation between BCL2
expression and overall survival within the GCB subgroup
but that BCL2 expression has a significant adverse effect on
overall survival within the non-GCB subgroup.10,26Unfor-
in consultation from other institutions, and we do not have
adequate clinical or survival data to comment on prognosis.
Rearrangement of MYC at band 8q24, a characteristic
event in Burkitt lymphoma, has been reported in
approximately 15% of DLBCL cases in Western countries
and has been associated with a poor clinical outcome.2
MYC plays a role in the pathogenesis of DLBCL by
promoting cell-cycle progression and tumor proliferation.
In this study, the frequency of MYC rearrangement was
30%, double of that reported in Western populations.
These are additional data to implicate geographic or
genetic differences between DLBCL in northern China
and in Western countries. Our study group (n 5 27) is
small, however, and this observation needs to be
confirmed in larger studies. In our group of Chinese
patients with DLBCL, there was no significant difference
in the frequency of MYC rearrangement between the GCB
and non-GCB subgroups.
Inactivation of the p53 tumor suppressor gene is
recognized as a key step in the development of 50% to
60% of human malignancies. p53 gene mutations have
been observed in 20% to 45% of patients with DLBCL.6,28,29
p63, a member of the p53 tumor suppressor gene family,
with structural homology to p53, is essential for healthy
embryonic development and is thought to behave as an
oncogenic molecule when overexpressed.28,30In contrast
with p53, which is immunohistochemically undetectable
or very weakly expressed in healthy tissues and which
reaches detectable levels only after mutational inactiva-
tion or genotoxic stress, p63 exhibits a consistent expres-
sion pattern in certain normal tissues.30p63 is expressed at
high levels in stratified epithelial cells and in their
corresponding tumors, and p63 is also expressed at low
to moderate levels in a subset of germinal center cells in
lymph nodes.30Only small amounts of data are available
on p63 expression in malignant lymphomas. One study
from the United States reported that p63 was expressed in
32% of DLBCLs.29Other groups from Brazil and Korea
found that p63 was expressed in 15% and 53% of DLBCLs,
respectively.28,31The Korean group further noted that p53
and p63 were both expressed in 30% of cases and that
patients with p63 overexpression showed significantly
poorer rates of survival.28They speculated that p63 could
act as an oncogene by inhibiting p53 function in DLBCL.
Similar to what was reported from Korea, we found that
48% of the patients in our case study had p53 overexpres-
sion, 57% had p63 overexpression, and 33% expressed
both p53 and p63. The higher expression and coexpression
of these 2 proteins in Chinese patients with DLBCL may
suggest a role in pathogenesis.
In conclusion, we have identified differences between
cases of DLBCL in northern China and that reported for
DLBCL cases in Western countries. In particular, the
frequency of the GCB type is less, BCL6 is less frequently
expressed or is rearranged, and MYC is more often
rearranged in patients with DLBCL in China compared
with Western countries. The relatively high frequency of
overexpression of p53 and p63 in this case series,
compared with DLBCL cases in other countries, is also
of interest, raising the possibility of a role for this pathway
in the pathogenesis of DLBCL from China.
This study was supported by a scholarship from the Chinese
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